Feeding is inhibited by sublethal concentrations of toxicants and by heat stress in the nematode Caenorhabditis elegans: Relationship to the cellularstress response
D. Jones et Epm. Candido, Feeding is inhibited by sublethal concentrations of toxicants and by heat stress in the nematode Caenorhabditis elegans: Relationship to the cellularstress response, J EXP ZOOL, 284(2), 1999, pp. 147-157
We report that the free-living nematode Caenorhabditis elegans can respond
to a variety of stressors (compounds known to induce the production of cell
ular stress proteins in model biological systems), by ceasing pharyngeal pu
mping. This phenomenon results in both a reduction in intake of the stresso
r and a cessation of feeding. The effect of stressors can therefore be conv
eniently assayed by monitoring the decrease in the density of the bacterial
food in liquid cultures of nematodes. A great range of stressors induced t
his response including alcohols, heavy metals, sulfhydryl-reactive compound
s, salicylate, and heat. For several of these stressors, inhibition of phar
yngeal pumping occurred at stressor concentrations below the threshold requ
ired for the induction of the 16-kDa heat shock proteins. Salicylate, which
did not induce 16-kDa heat shock proteins at any concentration, neverthele
ss inhibited pharyngeal pumping. Heat was also inhibitory, at a temperature
where 16-kDa heat shock protein production was near maximal. Some compound
s caused only a partial inhibition of feeding while with others the effect
was complete. Upon removal of the stressor, the nematodes resumed pharyngea
l pumping with a residual inhibitory effect that depended on the concentrat
ion and type of stressor that had been applied. A number of C. elegans neur
osensory mutant strains also exhibited a cessation of pharyngeal pumping wh
en exposed to stressors suggesting that the mechanism underlying this inhib
ition was not entirely neurosensory and may be intrinsic to the pharynx. In
C. elegans and other invertebrates, stress-induced inhibition of feeding m
ay be an important survival mechanism that limits the intake of toxic solut
es. J. Exp. Zool. 284:147-157, 1999. (C) 1999 Wiley-Liss, Inc.